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. 2019 Sep 16;14:106. doi: 10.1186/s13000-019-0877-2

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — Over-expression of DNM3OS enhanced proliferation and suppressed apoptosis in CHON-001 cells, while DNM3OS silencing had opposite effects. (a) CHON-001 cells proliferation was improved by DNM3OS, while silencing DNM3OS inhibited CHON-001 cells proliferation as indicated by cloning formation experiment. (b) The number of proliferated cells was quantified. (c) CHON-001 cells apoptosis was inhibited by DNM3OS, while DNM3OS silencing induced apoptosis as indicated by flow cytometry. (d) The proportion of apoptosis was quantified. (e) The apoptosis-related proteins (Bcl-2, Bax and c caspase 3) were detected by Western blot. (f) The relative levels of proteins described in (e) were counted by GAPDH as normalization. ^aP < 0.05 vs. Blank, ^bP < 0.05 vs. NC, ^cP < 0.05 vs. DNM3OS, ^dP < 0.05 vs. siNC. siDNM3OS: small interfering dynamin 3 opposite strand; NC: negative control; Bcl-2: B-cell lymphoma-2; Bax: Bcl2-associated X protein